阿玛罗龙胆亭通过诱导结直肠癌中的铁死亡来抑制细胞增殖和上皮-间质转化过程。
Amarogentin suppresses cell proliferation and EMT process through inducing ferroptosis in colorectal cancer.
作者信息
Wang Chao, You Zihao, Zhou Guoqing, Dong Juanjuan, Tong Sihao, Sun Guoping
机构信息
Anhui Medical University, Hefei, 230022, China.
Department of Oncology, The First Affiliated Hospital of Anhui Medical University, Hefei, 230022, China.
出版信息
BMC Gastroenterol. 2025 Jan 30;25(1):46. doi: 10.1186/s12876-025-03649-w.
BACKGROUND
Colorectal cancer (CRC) is one common tumor with the high death rate, and badly affects the normal lives of CRC patients. Amarogentin (AG) has been found to exhibit regulatory roles and join into the progression of multiple diseases. However, the regulatory impacts and associated molecular mechanisms of AG in CRC progression keep unclear.
METHODS AND RESULTS
In this study, it was demonstrated that AG weakened CRC cell viability in a concentration- and time-dependent manner. In addition, AG accelerated cell apoptosis by triggering ferroptosis. The cell invasion and EMT process were restrained after AG treatment, but these impacts were reversed after Fer-1 addition. Moreover, it was uncovered that AG retarded Nrf2/HO-1/GPX4 activation. Additionally, AG modulated PTC cell viability and stimulated ferroptosis. At last, it was illustrated that AG suppressed tumor growth in vivo.
CONCLUSION
In conclusion, it was disclosed that AG suppressed cell proliferation and EMT process through inducing ferroptosis in CRC, and retarded Nrf2/HO-1/GPX4 activation. This discovery suggested that AG may be one effective drug for ameliorating CRC progression.
背景
结直肠癌（CRC）是一种常见的高死亡率肿瘤，严重影响CRC患者的正常生活。已发现阿玛罗苷（AG）具有调节作用，并参与多种疾病的进展。然而，AG在CRC进展中的调节作用及相关分子机制尚不清楚。
方法与结果
在本研究中，结果表明AG以浓度和时间依赖性方式削弱CRC细胞活力。此外，AG通过触发铁死亡加速细胞凋亡。AG处理后细胞侵袭和EMT过程受到抑制，但添加Fer-1后这些影响被逆转。此外，发现AG抑制Nrf2/HO-1/GPX4激活。此外，AG调节PTC细胞活力并刺激铁死亡。最后，表明AG在体内抑制肿瘤生长。
结论
总之，研究表明AG通过诱导CRC中的铁死亡抑制细胞增殖和EMT过程，并抑制Nrf2/HO-1/GPX4激活。这一发现表明AG可能是一种改善CRC进展的有效药物。
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